Longitudinal bone growth occurs at the growth plate, a thin layer of cartilage which consists of three principal zones: the resting zone, the proliferative zone, and the hypertrophic zone. With age, growth plate chondrocyte proliferation slows down, causing longitudinal bone growth to slow and eventually stop. Our previous studies suggest that proliferation slows because stem-like cells, located in the resting zone of the growth plate, have a finite proliferative capacity which is gradually exhausted. However, if resting zone chondrocytes are placed in cell culture they can be induced to proliferate substantially, even if the donor animal was older, near the end of longitudinal bone growth. This finding raises the possibility that the loss of proliferative potential is context-dependent and reversible. We have also shown that growth plate senescence is associated with loss of DNA methylation in resting zone chondrocytes, suggesting that growth plate senescence may involve epigenetic changes. Another possible mechanism that could contribute to growth plate senescence involves telomere shortening. To test this hypothesis, we compared the telomere restriction fragment (TRF) length in resting zone chondrocytes of Mus casteneus at 1, 4, 8, and 56 weeks of age. We found that TRF length did not diminish measurably with age, suggesting that telomere shortening in resting zone chondrocytes is not the mechanism that limits proliferation of growth plate chondrocytes in vivo. In children, after a period of growth inhibition, the linear growth rate usually exceeds the normal range. This phenomenon, known as catch-up growth, has been observed in humans and other mammals, following a wide variety of growth-inhibiting conditions. We have shown evidence that catch-up growth is not due to a hormonal or other systemic mechanism but rather to a local mechanism intrinsic to the growth plate. In particular, our findings suggest that catch-up growth occurs because growth-inhibiting conditions slow growth plate chondrocyte proliferation, thus conserving the proliferative capacity of the chondrocytes, and consequently slowing senescence. As a result, following transient growth inhibition, growth plates retain a greater proliferative capacity, are less senescent, and hence show a greater growth rate than expected for age, resulting in catch-up growth. We conducted a clinical study to determine whether the pattern of catch-up growth in children is consistent with the delayed senescence hypothesis. If catch-up growth is due solely to a delay in growth plate senescence, then the linear growth rate of a child experiencing catch-up growth should be equal to the growth rate of a normal younger child. Thus, the growth curve during catch-up growth should represent a simple time-shift of the normal growth curve of a younger child. To test this theory we analyzed catch-up growth in children with celiac disease placed on a gluten-free diet. At onset of the gluten-free diet, the average height age and bone age were delayed by 0.7 years. Mathematical analysis showed that the growth rate over the ensuing 36 months was increased for chronological age, but the growth pattern was normal for a child 0.7 years younger. These findings are consistent with the hypothesis that catch-up growth is due to delayed senescence of the growth plate.